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Inflammatory Disorders of the Salivary Glands
Key Points
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Sialadenitis, most commonly caused by sialolithiasis, should be treated medically in the acute care setting with warm compresses, sialogogues, hydration, and antibiotics. Chronic or persistent disease may require minimally invasive sialendoscopy for diagnostic and therapeutic purposes.
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Sialendoscopic techniques include endoscopic visualization of stenosis or calculi, balloon dilatation of stenoses, fragmentation of large stones with Holmium laser, and ensnarement of stones with a wire basket.
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Although imaging (ultrasound, computed tomography, or magnetic resonance imaging) is an appropriate ancillary test for many cases of sialadenitis, the diagnosis of most viral (mumps, HIV) and granulomatous (actinomycosis, cat scratch disease, toxoplasmosis) salivary gland infections requires specific serology antibody testing, skin testing, or fine-needle aspiration.
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Sjögren syndrome, a chronic autoimmune disorder characterized by destruction of the bilateral salivary and lacrimal glands that leads to dry mouth and dry eyes, is managed with symptomatic treatment (salivary substitutes, sialogogues, frequent dental examinations, eye drops, and lubricants). Some patients with recurrent sialadenitis may benefit from dilation of salivary gland ducts or possibly even gland excision.
Inflammatory disorders of the salivary glands can vary in their cause, chronicity, treatability, and overall prognosis. The most common cause is obstruction of salivary outflow, most commonly from a sialolith in the duct. Salivary gland infections—including bacterial, viral, fungal, parasitic, and protozoal infections—are another major cause of sialadenitis. Additionally, systemic medical pathologies, such as autoimmune diseases like Sjögren disease, can also affect the salivary glands.
Sialolithiasis
Sialolithiasis is the formation of calculi in the ductal system of the salivary glands. It is the most common cause of inflammation in the salivary glands. The submandibular gland is most commonly affected, and 80% to 90% of stones develop in the Wharton duct. Approximately 10% to 20% of calculi form in the parotid (Stensen) duct, and 1% form in the sublingual duct. Patients in their fifth to eighth decades of life represent most cases. Sialolithiasis in children is rare; however, if afflicted, they most commonly come to medical attention at about 10 years of age. Men tend to develop calculi more frequently than women.
Salivary stones are composed predominantly of calcium phosphate and carbonate in combination with an organic matrix of glycoproteins and mucopolysaccharides. Small amounts of other salts such as magnesium, potassium, and ammonium are also involved in stone formation.
The precise etiology of sialolithiasis remains unknown. Salivary stasis and inflammatory changes to the ductal system are important factors that contribute to stone formation. It is believed that intermittent salivary stasis results in an alteration of the mucoid elements of saliva, which leads to the formation of an organic gel. This gel becomes the framework for the deposition of salts, which leads to the development of calculi. Serum levels of calcium and phosphorous do not seem to be related to stone formation.
The relationship between sialolithiasis and chronic sialadenitis might differ among salivary glands. In the submandibular gland, development of a sialolith might be the primary event that results in stagnation of saliva and inflammation, which encourages retrograde bacterial migration that can result in sialadenitis. In contrast, inflammation and ductal injury in the parotid gland from chronic sialadenitis is believed to be the inciting process for sialolithiasis. Additionally, several other factors might account for the propensity of salivary stones to form in the submandibular gland. The Wharton duct is longer, wider, more tortuous, and angulated against gravity as it courses around the mylohyoid muscle; all of these contribute to slower salivary flow rates and consequently poor salivary egress into the oral cavity and thus promote stasis. Also, the saliva produced by the gland itself is more viscous and has a higher calcium and phosphorous concentration. In the parotid gland, stones are most commonly located at the hilum or parenchyma. Sialolithiasis in the submandibular gland tends to develop in the duct.
Patients with sialolithiasis are seen with recurrent episodes of postprandial salivary colic with pain and swelling. The patient might also have a history of multiple cases of acute suppurative sialadenitis. On physical examination, bimanual palpation sometimes reveals the presence of a palpable stone involving the submandibular duct. Parotid stones might be noted at the orifice of the Stensen duct or along the course of the duct. Examination may also reveal asymmetric findings in the patency of salivary ducts and quality of saliva, and obstructed ducts may show lack of salivary flow on bimanual palpation or massage of the gland, or they may demonstrate mucoid, particulate, or mucopurulent saliva. Consequently, patients will frequently come in with symptoms of foul-tasting fluid on massaging the obstructed gland that can point to the etiology of the symptoms.
Imaging of the salivary glands for sialolithiasis may be accomplished with ultrasound, computed tomography (CT), or magnetic resonance imaging (MRI). Plain radiographs that use intraoral or occlusal views were traditionally helpful for identification of radiopaque stones but are no longer routinely used because they miss radiolucent stones and can confuse sialoliths with other calcifications in the area such as phleboliths, atherosclerosis of the lingual artery, or calcified cervical lymphadenopathy.
Instead, newer imaging techniques are commonly used. Ultrasound has proven value in the diagnosis of sialolithiasis and has the ability to detect 90% of stones greater than 2 mm. Although the accuracy of ultrasound is dependent on the operator, in general, it is very useful for several reasons. Ultrasonography is cost-effective, avoids radiation exposure, is repeatable and dynamic, provides excellent definition of the salivary gland and mobility of the calculus, and also can be utilized intraoperatively for stone localization. CT scanning with fine cuts (1 to 2 mm) is extremely accurate at detecting salivary stones. Contrast is avoided, because opacified blood vessels can be confused with sialoliths. However, the physician must not ignore the possibility of a synchronous neoplastic process. Consequently, in cases where the history, physical examination, or other radiologic findings are suspicious of a neoplastic process in addition to an inflammatory condition, a CT scan with and without contrast should be obtained. Findings typically include an enlarged gland and dilatation of the duct ( Fig. 83.1 ).
On MRI, the calculus is seen as a low signal intensity focus on both T1- and T2-weighted images. Digital subtraction sialography, which lessens the interference of surrounding bony structures, can also be used to investigate sialolithiasis, because it can detect radiolucent stones with a reported sensitivity of 95% to 100%. Several disadvantages are inherent to sialography. It is an invasive technique with the possible side effects of contrast material. Sialography is also contraindicated for stones located in the oral portion of the Wharton duct and in cases of active infection. MR sialography, which uses saliva as the contrast medium, is a relatively new and noninvasive technique used to evaluate the salivary duct system ( Fig. 83.2 ). Studies indicate that MR sialography of the submandibular duct with evoked salivation has accuracy similar to that of digital sialography and is superior to ultrasound. MR sialography is a better alternative in patients with contraindications to digital sialography. However, pathologic diagnosis in this setting is difficult, and the ductal metaplasia of sialolithiasis secondary to stone formation might be misinterpreted with mucoepidermoid carcinoma. Ultrasonography and CT scanning are first-line imaging techniques for evaluation and management of sialolithiasis. MRI sialography, digital sialography, and three-dimensional reconstructions to facilitate virtual salivary endoscopy are reserved for complex cases.
Management of salivary stones depends on the size, location, orientation, shape, number, whether the stone is impacted or mobile, and the surgeon's experience. Additionally, the earlier the stone is removed, the better the prognosis, because the longer stones occupy ducts, the larger and more immobile they may become.
Initial nonsurgical management of patients with sialolithiasis consists of the use of sialagogues, local heat, hydration, and massage of the involved gland. If salivary gland infection is suspected, prompt antimicrobial therapy should be initiated.
Surgical intervention for sialolithiasis depends on the anatomic location of the stone. Submandibular stones that are palpable in the mouth and no more than 2 cm from the duct orifice distal to the posterior edge of the mylohyoid muscle can sometimes be removed by simply milking the stone through the duct opening manually or making a transoral incision. Traditionally, proximal, hilar, or intraglandular stones; impacted stones; and large stones or megaliths in the submandibular gland would be managed with a submandibular gland resection. The anatomy of the Stensen duct makes the management of parotid stones more difficult, because manipulation of the duct may be complicated by a high incidence of stricture and frequently requires the use of a temporary stent. However, the traditional management of parotid stones includes transoral approaches, continued medical management, or parotid gland excision.
Salivary endoscopy has caused a paradigm shift in the management of salivary stones. Today, using a combination of endoscopic techniques combined with transoral or external approaches, also known as combined or hybrid techniques, it is possible to provide a safe, effective, gland-preserving alternative with success rates between 80% and 100%. Sialendoscopy uses miniature, semirigid endoscopes that range from 0.8 to 1.6 mm in size and have an interventional irrigation port that permits intervention using a variety of tools to manage salivary stones and other obstructive pathology, such as stenosis ( Fig. 83.3 ). A variety of interventional tools have also been developed to provide fast and nontraumatic dilation of the salivary ducts and papillae to facilitate the introduction of the endoscope and instruments into the cannulated papilla and the ductal system. Salivary endoscopy has gained popularity recently as a diagnostic and therapeutic tool. Stones and strictures can be directly visualized, and stones can be removed using a wire basket to ensnare them; if the stones are too large for the wire basket, they may be fragmented into smaller pieces using a holmium laser or lithotripsy ( Fig. 83.4 ).
If this proves ineffective or the stone is impacted, the combined approach with an external incision can be used. The combined approach involves visualization and localization of the stone by endoscopy or ultrasound and removal of the stone by making an incision into the duct. When exploring the duct, submandibular stones can be excised via an intraoral approach; however, parotid stones may require a partial or complete parotidectomy incision and elevation of the superficial musculoaponeurotic system flap to gain access to the stone. At the conclusion of the procedure, a salivary stent may be left in place for 2 to 4 weeks to prevent stenosis or stricture of the duct or papilla.
Chronic Sialadenitis
Chronic sialadenitis is a localized condition of the salivary gland characterized by relapsing and remitting episodes of pain and inflammation. The submandibular gland is the most frequently affected site. The initial inciting factor is believed to be salivary duct obstruction, which results in salivary stasis and eventually in ascending bacterial infection. The most common cause of ductal obstruction is sialolithiasis. Additional causes include stricture of the salivary duct, extrinsic compression by tumor, stenosis secondary to scar in adjacent tissue, congenital dilation, and foreign body. Salivary stasis from obstruction predisposes patients to episodes of infection and inflammation. Recurrent inflammatory reactions result in multifocal wall irregularities, which consequently form strictures. Chronic inflammation can also cause progressive acinar destruction with fibrous replacement, thereby resulting in glandular atrophy and sialectasis.
Clinically, patients experience recurring episodes of sudden-onset swelling and tenderness of the affected gland. A low-grade fever can occur in association with episodes, and no known relationship with meals or seasons has been found. Patients frequently report an initial episode of acute suppurative (bacterial) sialadenitis; asymptomatic intervals might range from a few weeks to months. Physical examination reveals enlargement of the gland, and frequently mucopus may be seen draining from the ductal orifice. Mucopus is more viscous than saliva, and it results in obstruction of the ductal lumen and salivary stasis. Occasionally, pus can be viewed in patients with chronic sialadenitis, but this is probably an acute bacterial sialadenitis superimposed on the chronic condition. Staphylococcus aureus is the most common causative microorganism involved in adults.
Initial treatment is conservative and involves oral antibiotics, massage, heat, sialogogues, and corticosteroids. Antibiotics are only effective if acute sialadenitis is present. Corticosteroid taper can be used in the short term to decrease inflammation, and hydration via sialogogues and warm compresses serve to flush out the precipitated serum proteins within the salivary ducts. If this treatment fails, sialendoscopy can be used to wash out the intraductal system and dilate the ducts. Sialendoscopy serves as a diagnostic and interventional tool. Generally, if the patient suffers from more than one acute attack per year, interventional sialendoscopy may be considered.
Diagnostic endoscopy can improve symptoms by washing out the salivary ducts with a continuous normal saline lavage, intraglandular steroid instillation, and hydrostatic dilation of the ductal system. Salivary stenoses diagnosed on endoscopy require further management depending on the severity, location, and length of the stenosis. Salivary stenosis can be dilated endoscopically using balloon dilators or combined approach techniques ( Figs. 83.5 and 83.6 ).
Additionally, stents may be used to prevent stricture reformation and can be kept in place for up to 4 weeks ( Fig. 83.7 ). If the previous methods prove ineffective, a final strategy is surgical removal of the gland. Invasive techniques to induce gland atrophy, such as tympanic neurectomy and parotid duct ligation, are rarely if ever performed.
Patients with chronic sialadenitis typically show punctate sialectasis and dilation of the peripheral ducts on imaging. Imaging modalities include ultrasound, CT, conventional MRI, and MRI sialography. Ultrasonography can be used to visualize both dilatated ducts and calculi while the patient is in the clinic; it has also been used intraoperatively to aid in visualization of the ductal system.
Possible complications of chronic sialadenitis include the development of a benign lymphoepithelial lesion, Küttner tumor, and ductal carcinoma. A benign lymphoepithelial lesion is characterized by a lymphoreticular infiltrate with acinar atrophy, irregularly placed nuclei, and ductal metaplasia; the metaplasia results in the development of epimyoepithelial islands. Women in the fifth to sixth decades of life are more commonly affected, and a benign lymphoepithelial lesion has been associated with Sjögren syndrome and has also been termed Mikulicz disease . A benign lymphoepithelial lesion typically presents as an asymptomatic mass. Fine-needle aspiration (FNA) may be used for diagnosis and allows for a nonsurgical approach to management. However, patients must be followed because of reports of malignant transformation.
Küttner tumor, or chronic sclerosing sialadenitis , is a benign chronic inflammatory process similar to a benign lymphoepithelial lesion. However, the lesion occurs almost exclusively in the submandibular gland and is characterized by a progressive fibrosis and parenchymal atrophy. Küttner tumors are most common in the fifth through seventh decades of life, and women have a slightly higher incidence of occurrence. The clinical presentation involves firm, painful swelling of the gland that is usually unilateral. Periductal fibrosis and ductal ectasia occur in early stages of the disease, caused by foci of chronic inflammation. However, as the disease progresses, fibrosis, acinar atrophy, and ductal dilation increase. Consequentially, the entire gland becomes fibrotic, and inflammation decreases. Histologically, a heavy lymphoid infiltrate is found among discrete tubular structures with regularly aligned nuclei, which differentiates them from a benign lymphoepithelial lesion. Again, careful and routine assessment of patients with chronic sialadenitis is underscored by reports of the development of malignancies that include salivary ductal carcinoma. Symptomatic management of Küttner tumor can be accomplished by sialendoscopy to remove sialoliths using a wire basket to retrieve stones. Unfortunately, many of these patients need definitive treatment with gland excision, especially in later stages of the disease. Sarcoidosis, lymphoepithelial sialadenitis, and follicular lymphoma are included in the differential diagnosis.
Infections of the Salivary Glands
Salivary gland infections have a wide range of presentations, depending on the etiologic agents involved and the chronicity of the infection. These might range from acute localized infections, such as bacterial sialadenitis, to systemic diseases caused by viruses such as the paramyxovirus or the human immunodeficiency virus (HIV). Granulomatous infections might manifest as solitary masses similar to a neoplasm. In chronic infections, ductal obstruction might be a predisposing factor.
Acute Suppurative (Bacterial) Sialadenitis
Acute sialadenitis is typically a bacterial inflammation of the salivary glands, which appears as rapid, diffuse swelling and pain over the affected gland in addition to systemic manifestations such as fever, chills, and malaise. Acute infection of the salivary glands is caused by retrograde bacterial contamination of the salivary ducts from the oral cavity. Stasis of salivary flow secondary to dehydration or significant hemorrhage permits retrograde migration of bacteria and produces suppurative infection of the gland parenchyma. The parotid gland is most susceptible to such infections, a fact attributed to the difference in saliva composition among the various glands. The parotid gland produces saliva that is mainly serous, whereas saliva from the submandibular and sublingual glands is primarily mucoid. Serous saliva, unlike mucinous saliva, lacks lysosomes, immunoglobulin A antibodies, and sialic acid, all of which have antimicrobial properties. In addition, the saliva from the submandibular and sublingual glands contains high-molecular-weight glycoproteins that competitively inhibit bacterial attachment to the epithelial cells of the salivary ducts. Several predisposing factors might lead to acute sialadenitis. These include diseases such as diabetes mellitus, hypothyroidism, renal failure, and Sjögren syndrome. In addition, medications can reduce salivary flow through multiple mechanisms ( Fig. 83.8 ).
Mechanical impairment of salivary flow also predisposes to acute infection. Stenosis of the salivary ducts secondary to trauma or a foreign body has been reported to result in acute sialadenitis. Sialolithiasis, more frequent in the ducts of the submandibular and sublingual glands, might also contribute to acute infection but more commonly produces chronic salivary gland infection. Acute bacterial submandibular sialadenitis is a community-acquired disease that most commonly occurs from a sialolith in the Wharton duct (see the section on sialoliths for more information).
Sialadenitis has also commonly been associated with medically debilitated and postoperative patients. The incidence of acute sialadenitis is approximately 0.173 cases per 10,000 operations (0.00173%). Patients undergoing major abdominal and hip repair surgery have been identified as being at increased risk for acute suppurative sialadenitis, which is attributed to postoperative dehydration. The disease is most commonly reported to occur within the first two postoperative weeks.
The elderly are at a higher risk of developing sialadenitis, often because of a medication-induced decrease in salivary flow. Drugs that contribute to salivary stasis include anticholinergics and antihistamines. Other predisposing factors to sialadenitis include dehydration, poor oral hygiene, immunosuppression, salivary duct obstruction, autoimmune diseases (Sjögren syndrome), diabetes mellitus, hypothyroidism, and renal failure. Of the medically ill patients affected by sialadenitis, approximately 25% have a malignant lesion, and another 50% have a preexisting infection elsewhere than the head and neck. Most affected patients are between 50 and 60 years of age; men have a higher incidence, and the right side is involved more frequently than the left.
The past few decades have brought change to the bacterial flora of the oral cavity, which affects the management of acute bacterial parotitis. This has occurred for several reasons, among which is the increase in nosocomial and opportunistic infections among immunocompromised and ill patients admitted to the hospital. Additionally, improved technology has allowed for the culture and accurate identification of more microorganisms, especially anaerobes. Finally, the abundant use of oral antibiotics in the community has resulted in microorganisms that can survive in the oral cavity that normally would not. In addition, antibiotic resistance occurs in organisms that normally occupy the oral cavity. The most common pathogens associated with acute bacterial parotitis are S. aureus and anaerobic bacteria such as Fusobacterium and Peptostreptococcus (gram-negative bacilli). Additionally, streptococcal species and aerobic gram-negative bacilli have been reported. Nosocomial parotitis is associated with aerobic and facultative gram-negative bacteria, as well as S. aureus , so methicillin resistance should be investigated.
On physical examination, the patient might demonstrate signs of systemic dehydration with dry mucous membranes. Local findings include tenderness to palpation with warmth and induration of the overlying skin. Bimanual palpation of the gland results in suppurative discharge from the red and distended duct orifice in approximately three-fourths of cases. Multiple glands might be affected, with a reported incidence of bilateral involvement in up to 25% of cases.
The laboratory evaluation typically reveals a leukocytosis with neutrophilia. Also, signs consistent with dehydration may occur, such as hypernatremia and elevated blood urea nitrogen. Imaging of the affected gland with CT or ultrasound for abscess formation is indicated in patients who do not respond to medical therapy within 48 to 72 hours. Sialography performed in the acute phases of sialadenitis provides little useful information and is contraindicated because it can exacerbate the existing inflammation. However, ultrasonography, CT, and MRI may be used if neoplasms, sialolithiasis, or abscesses are suspected.
If there is active drainage from the duct, it can be cultured to further direct antimicrobial therapy; however, a risk of contamination from the oropharynx exists when culturing purulent discharge from the Stensen duct. Moreover, caution should be used during FNA of the parotid gland because a granulomatous infection can result in fistula formation. Cultures should be tested for aerobic and anaerobic bacteria, fungi, and mycobacteria.
Although the diagnosis of acute parotitis is usually apparent, the differential diagnosis for nonparotid swelling that mimics parotitis includes lymphoma, lymphangitis, external otitis, Bezold abscess, cervical adenitis, dental abscesses that appear as buccal or masseteric space abscesses, and infected branchial cleft or sebaceous cysts.
Initial treatment of acute suppurative sialadenitis begins with aggressive medical management. This includes prompt fluid and electrolyte replacement, antibiotic therapy, oral hygiene, and reversal of salivary stasis. Stimulation of salivary flow is accomplished by the use of sialogogues such as lemon drops and orange juice. In addition, capable patients should be instructed on regular external and bimanual massage, starting from the distal bed of the gland and progressing toward the papillae. Analgesics and local heat application ease the discomfort.
Antimicrobial therapy is an essential part of the management of acute salivary gland infections. Antimicrobial therapy is initiated empirically toward gram-positive and anaerobic bacteria. However, the recovery of β-lactamase–producing bacteria in 75% of patients requires the use of augmented penicillin and antistaphylococcal penicillin or a first-generation cephalosporin. Culture results should be used to further direct antimicrobial treatment. Methicillin-resistant S. aureus infection may require the use of vancomycin or linezolid. The use of clindamycin or the addition of metronidazole to the first-line agents to broaden anaerobic coverage has been advocated by some authors. Response to antimicrobial therapy is seen within 48 to 72 hours of initiating treatment and should continue for 1 week after resolution of symptoms.
Rarely, conservative measures fail to eradicate the infection, and surgical drainage of a loculated abscess is necessary. The surgical approach involves elevation of an anterior-based facial flap with abscess drainage by way of radial incisions in the parotid fascia parallel to the facial nerve branches. A drain should be placed, and wound edges should be loosely approximated; the central aspect is left to heal by secondary intention.
Sialendoscopy is generally contraindicated in acute sialadenitis, because inflammation of the ducts makes dilation difficult and increases the risk of iatrogenic ductal trauma from rigid and semirigid instrumentation. Exacerbation of the infection is also a potential risk.
Complications of acute suppurative parotitis are unusual. Suppuration usually confined to the duct lumen might eventually erode through the epithelium into the interstices of the parenchyma, creating multiple small abscesses that might coalesce into larger collections that can infiltrate a number of potential spaces of the neck. Osteomyelitis, thrombophlebitis of the jugular vein, septicemia, respiratory obstruction, and death are potential sequelae of suppurative parotitis. Rupture through the floor of the external auditory canal; spontaneous drainage through the cheek; and extension to the face, neck, and mediastinum have also been reported. Facial nerve paralysis, whether complete or incomplete, is uncommon. The etiology of paralysis is unknown but is thought to be due to perineuritis, the virulence of the offending organisms, or acute nerve compression. Facial nerve paralysis with a palpable mass is highly suggestive of an underlying malignancy, and this must be ruled out until resolution of the inflammatory process with full recovery of nerve function.
Neonatal Suppurative Parotitis
Infections of the salivary glands are uncommon in the neonate. When infections do occur, they are termed neonatal suppurative parotitis (NSP), and the parotid gland is most often involved. Salivary gland infection is more common in preterm and male neonates, as are dehydration and nasogastric feeding. S. aureus is the most common pathogen, but group B and viridans streptococci, Streptococcus pyogenes , Peptostreptococcus and Staphylococcus species (coagulase-negative), Bacteroides melaninogenicus , and Fusobacterium nucleatum have also been implicated in NSP. The oral cavity is replete with anaerobic bacteria and serves as the portal of entry in most patients through retrograde transmission of bacteria. This is especially common in the event of salivary stasis or dehydration. However, blood-borne bacteria, most commonly gram-negative bacteria, might infect the salivary glands.
In addition to fever, anorexia, irritability, and lack of weight gain, other clinical signs of NSP can include swelling and erythema of the skin overlying the involved gland. Swelling is usually unilateral initially but often becomes bilateral. The gland might be tender, and the swelling can be firm or fluctuant.
Diagnosis of NSP is made on the basis of clinical findings and Gram stain and culture of pus from the duct or from FNA of the gland. Laboratory findings include a leukocytosis with neutrophilia. Serum amylase levels are usually normal, possibly because of immature salivary isoenzyme activity. Ultrasonography shows an enlarged gland with hypoechoic areas. Initial therapy consists of hydration and parenteral antibiotics directed at S. aureus and gram-negative bacilli until culture and sensitivity results are available. The presence of methicillin-resistant staphylococci cannot be ruled out. Drainage procedures should be used only when prompt clinical improvement does not occur, when fluctuance of the gland increases, or with an intraparotid abscess.
Recurrent Parotitis of Childhood
Recurrent parotitis of childhood (RPC) is a rare, nonspecific sialadenitis of the parotid gland characterized by periodic episodes of swelling and pain that typically resolves spontaneously prior to the onset of puberty. It is the second most common inflammatory salivary gland disease of childhood after mumps. Clinically, patients are seen with recurrent episodes of acute or subacute parotid gland swelling along with fever, malaise, and pain, frequently after a meal. Episodes of RPC are commonly unilateral; if involvement is bilateral, the symptoms are more prominent on one side. Afflicted patients tend to experience exacerbations every 3 to 4 months, and each might last days to weeks. The first signs manifest during the first 1 to 2 years of life, but the disease is usually not diagnosed until after three to four episodes by the age of 3 to 6 years. Boys are more frequently affected than girls. Although it almost always universally resolves during puberty, RPC can lead to severe destruction of the glandular parenchyma with a functional loss of 50% to 80%. Thus the need to detect and treat early is paramount.
Risk factors include congenital abnormalities or strictures of the Stensen duct and a history of viral mumps, trauma, or foreign bodies within the duct. Evidence also suggests that upper airway infections result in dehydration, which can fuel subsequent flare-ups.
The cause of RPC remains unknown, although multiple etiologies have been proposed. Several authors advocate that congenital ectasia of portions of the secondary ductal system predisposes children for bacterial colonization that leads to recurrent parotitis. S. aureus and Streptococcus viridans are the most commonly isolated organisms from the parotid ducts of patients. A familial form of RPC has been described with autosomal inheritance. Immunologic abnormalities with isolated deficiencies in immunoglobulins G3 and A have been associated with recurrent parotitis. In addition, parotid swelling might be the sole manifestation of juvenile-onset primary Sjögren syndrome. Several viruses might also play a role in RPC. A history of mumps parotitis often exists, and repeated multiplication of the Epstein-Barr virus (EBV) in the parotid gland might be responsible for establishing recurrent parotid gland inflammation; RPC has a reported incidence of 20% in HIV-infected children.
The histologic appearance of affected parotid glands demonstrates massive periductal lymphocytic infiltration. The intraglandular ducts are dilated and measure approximately 1 to 2 mm in diameter.
Several imaging modalities may be used to study the ductal system of patients with RPC. The characteristic finding is sialectasis that on conventional sialography appears as numerous scattered, punctate pools of contrast. Ultrasonography of the parotid gland reveals an enlarged gland with multiple small hypoechoic areas. These areas represent both sialectasis of the ducts and surrounding lymphocytic infiltration. Recently, MR sialography has been reported to be useful in the evaluation of RPC. It is a noninvasive study that does not require contrast, and it may be used during acute episodes.
Treatment options range from observation with medical management to surgery. Initial treatment consists of adequate hydration, pain control, gland massage, local heat, sialogogues, and appropriate intravenous antibiotics. Empiric therapy before culture results should consist of a penicillinase-resistant antistaphylococcal antibiotic. Most patients experience rapid resolution of swelling and discomfort. For patients with persistent symptomology, interventional sialendoscopy may serve both diagnostic and therapeutic goals. The endoscopic view of a narrow duct with blanched ductal walls and loss of normal vascular markings is a characteristic finding ( Fig. 83.9 ).
Endoscopic findings include mucus plugs and strictures. These can be treated with high-pressure balloon dilation and endoscopic removal of debris or saline lavage. Endoscopic irrigation with cortisone and sodium chloride to decrease inflammation may also be beneficial. One treatment is to irrigate the glands with triamcinolone acetate (Kenalog); 40 units are diluted in 3 to 5 mL of normal saline after completion of endoscopy for patients with RPC. Sialography, which uses highly concentrated iodinated oil placed into the duct, may also serve both diagnostic and therapeutic roles because it uses an antiseptic solution for visualization of punctate sialectasis and dilation of peripheral ducts; the solution may linger in the duct for days or weeks and provides prolonged antiseptic effects. Instillation of sclerosing antimicrobials (tetracycline) can also be effective. Fortunately, virtually all cases resolve spontaneously with the onset of puberty or in late adolescence, and additional surgical treatment is rarely required.
Radioiodine-Induced Sialadenitis
Radioiodine has many uses in a variety of thyroid conditions, namely for treatment of thyrotoxicosis, for ablation of residual thyroid tissue after thyroidectomy, and in thyroid cancer surveillance. Some studies report that radiation-induced sialadenitis occurs in up to 18% to 26% of patients with thyroid carcinoma who receive radioactive iodine therapy. Others report subjective symptoms of sialadenitis, dry mouth, and dysgeusia in up to 60% of patients and abnormal scintigraphy in up to 69% of patients undergoing radioiodine therapy. Radioiodine-induced sialadenitis is characterized by an acute, diffuse parotid enlargement, which can be painful or painless. Bilateral involvement is reported most often. Toxicity to the salivary glands is dose dependent, and although toxicity related to lower doses (20 to 30 Gy) is reversible, higher doses (>50 Gy) carry the potential for irreversible damage. Symptoms can be debilitating and may significantly affect quality of life; these include chronic pain, constant or recurrent swelling of one or more glands, and dry mouth that causes odynophagia and dysphagia. Because the parotid glands are more predisposed to developing severe sialadenitis, gland excision is a less desirable alternative because of the risk of facial nerve injury associated with gland extirpation for inflammatory salivary gland disease.
Sialendoscopy is a relatively novel approach in the treatment of radioiodine-induced sialadenitis, and success rates vary. An interventional sialendoscopy procedure similar to that performed for RPC involves gland washouts, removal of debris and mucus plugs, and dilation of the papilla, ducts, or strictures with or without stent placement; this treatment seems to provide symptomatic benefit and reduced frequency and intensity of symptoms. Published studies report success rates that range from 50% to 100% in terms of relieving patients’ symptoms with interventional salivary endoscopy.
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